Cardiac muscles contract when action potentials depolarize plasma membranes. Decreased cardiac contractility is associated with dysregulation of calcium homeostasis, changes in cAMP-dependent regulation of contractile proteins, and alterations in β-adrenoceptor activity.8 The most common causes of contractile dysfunction include coronary artery disease resulting in myocardial infarction, systemic hypertension, and valvular disease. Progressive contractile dysfunction leads to heart failure (HF).8
The central role of intracellular Ca2+ and cAMP in cardiac muscle contraction provides a basis for the classification of agents with positive inotropic effects as (1) cardiac glycosides, (2) β1-adrenoceptor agonists, and (3) phosphodiesterase inhibitors.8 Currently, a cardiac glycoside, i.e., digoxin, is the only drug in the top 300 that regulates cardiac contractility (Table 4).2,8,10 It inhibits Na+/K+-ATPase and thereby increases intracellular Ca2+ concentration in myocytes and exerts a positive inotropic effect.8
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